Pathology of

Hepatobilier System

dr. Hermawan Istiadi, M.Si.Med

Bagian Patologi Anatomi FK UNDIP
085740148700
hermawanistiadi@fk.undip.ac.id
 CONTENT
1. Normal Histology
2. Mechanisms of Injury and Repair
3. Liver Failure
4. Bilirubin, Bile Formation and Jaundice
5. Infectious Disorders
6. Alcoholic Liver Disease
7. Metabolic Liver Disease
8. Cholestatic Diseases
9. Circulatory Disorders
10. Hepatic Disease Associated with Pregnancy
11. Cholelithiasis
12. Cholecystitis
 SASARAN BELAJAR
Mahasiswa mampu :
• Menjelaskan anatomi, histologi dan fisiologi normal sistem
hepatobilier
• Menjelaskan mekanisme injury dan repair pada hepar
• Menjelaskan patofisiologi dan gambaran klinis liver failure dan
sirosis hepatis
• Menjelaskan patofisiologi Ikterus
• Membedakan manifestasi klinis berbagai penyakit pada sistem
hepatobilier
• Membedakan gambaran makroskopis dan mikroskopis berbagai
penyakit pada sistem hepatobilier
LIVER HISTOLOGY
• Vena centralis (CV) : cabang
terminal dari v.heptica, pusat
dari lobulus
• Vena Porta (PV), titik sudut
perifer lobulus hexagonal
• Parenkim (hepatosit) :
Centrolobulus, periportal
Zona 1 > 2 > 3 (blood suply)
• Anatomical : Lobulus
• Functional : Acinus
• Darah mengalir
(Porta, a.hepatica)
menuju sinusoid s/d
CV
• Hepatosit menjadi
dinding dari sinusoid
LIVER HISTOLOGY
Bile canaliculi –
canal of herings –
Bile ductule –
Teriminal bile duct –
Duktus Koledokus
 Mekanisme Injury dan Repair
Respon Hepatosit & Parenkim
• Reversibel : Akumulasi Lemak intrasel (steatosis) dan Bilirubin
(cholestasis)

Steatosis / Perlemakan hepar

 Mekanisme Injury dan Repair
Respon Hepatosit & Parenkim
• Reversibel : Akumulasi Lemak intrasel (steatosis) dan Bilirubin
(cholestasis)

Kolestasis
 Mekanisme Injury dan Repair
Respon Hepatosit & Parenkim
• Irreversibel : Nekrosis / apoptosis

Nekrosis Apoptosis
 Laboratory
Evaluation of
Liver Disease
 Mekanisme Injury dan Repair
Scar Formation and Regression
• Sel yang berperan : hepatic stellate cell
• Hepatic stellate cell : Lipid storing – proliferation : highly
fibrogenic myofibroblasts – Scar deposition
• Fibrogenic myofibroblasts conversion initiated by :
▪ Chronic inflammation
▪ Cytokine and chemokine production by Kupffer cells,
endothelial cells, hepatocytes, and bile duct epithelial
cells
▪ Disruption of the extracellular matrix
▪ Stimulation of stellate cells by toxins
 Liver Failure
• Most severe clinical consequence of liver disease
• 80% to 90% of hepatic functional capacity must be lost
before hepatic failure ensues
• Mortality rate in hepatic failure without liver
transplantation : 80%.
• Acute and Chronic Liver Failure
 Liver Failure
1. Acute Liver failure
• Associated with encephalopathy and coagulopathy,
occurs within 26 weeks, in the absence of pre-existing
liver disease - fulminant liver failure
• Caused by massive hepatic necrosis
• Induced by drugs, toxins, Virus (USA : acetaminophen,
Asia : Hep.B-C)
• Clinical Course :
▪ nausea, vomiting, and jaundice, enlarged liver
 Liver Failure
1. Acute Liver failure
• Clinical Course :
▪ Hepatic encephalopathy – Elevated amonia -
impaired neuronal function and cerebral edema -
rigidity and hyperreflexia, Asterixis, confusion, stupor,
coma, Die
▪ Coagulation defects - Coagulopathy
▪ Portal hypertension – within days to weeks
 Liver Failure
1. Acute Liver failure
• Clinical Course :
• Hepatorenal syndrome - decreased renal perfusion
pressure due to systemic vasodilation,
activation of renal sympathetic system
(vasoconstriction of afferent) and increased
activation of the renin/angiotensin axis
Massive necrosis,
liver is small (700g)
Liver Failure
 Liver Failure
2. Chronic Liver Disease
• Leading causes worldwide : hepatitis B-C, nonalcoholic
fatty liver disease, and alcoholic liver disease
• 12 Most common cause mortality in US, 1st Liver related
death
• Most often associated with cirrhosis
Cirrhosis: a condition marked by diffuse transformation of the entire
liver into regenerative parenchymal nodules surrounded by fibrous
bands and variable degrees of vascular (often portosystemic) shunting
“Not all cirrhosis leads to chronic liver failure and not all end-stage
chronic liver disease is cirrhotic”
 Liver Failure
2. Chronic Liver Disease
 Liver Failure
2. Chronic Liver Disease
Regression of fibrosis, Uncommon, Rare

Pseudolobulus, thick collagen

 Liver Failure
2. Chronic Liver Disease
Clinical Features :
• 40% - asymptomatic until advanced stages
• Jaundice, encephalopathy, coagulopathy
• Pruritus
• Hiperestrogenemia - palmar erythema, spider
angiomas, infertilitas, steroid ↓, hypogonadism and
gynecomastia
• Portal Hypertension (Tekanan v.porta normal : 50-100
mmH2O, pada HP melebihi 500 mmH2O)
 Liver Failure
2. Chronic Liver Disease

Penyebab
Hipertensi
Portal
Liver Failure
Gambaran Klinis
Hipertensi Portal
• 85% ascites, caused by
Cirrhosis
• > 500 mL = detectable
• Mechanism :
• Hypoalbuminemia
• Hepatic lymph fow into
the peritoneal cavity (800
mL/day → 20 L/day)
• Splanchnic vasodilation
and hyperdynamic
circulation - activation RAS
Liver Failure
Gambaran Klinis
Hipertensi Portal

Portosystemic Shunts
• Dilation of collateral
vessels
• Venous bypasses develop
wherever the systemic and
portal circulation share
common capillary beds :
rectum (hemorrhoids),
esophagogastric junction
(varices), retroperitoneum,
abdominal wall (caput
Liver Failure

Esophageal
 Liver Failure
Gambaran Klinis
Hipertensi Portal

Esophageal Varices
• > 65% dari pasien Sirosis
Hepatis
• Sign : asimptomatik
hingga ruptur,
Hematemesis (< 50%)
• Ketika ruptur, 20% -30%
pasien meninggal dalam
serangan pertama
• Ketika ruptur, jika survive,
70% ruptur lagi dalam 1
 Liver Failure
Gambaran Klinis
Hipertensi Portal

Hepatopulmonary syndrome
• 30% patients cirrhosis and
portal hypertension
• Intrapulmonary vascular
dilations
• Blood flows rapidly -
inadequate time for oxygen
diffusion – hypoxia -
dyspnea
 Liver Failure
Gambaran Klinis
Hipertensi Portal

Portopulmonary
hypertension
• Pulmonary arterial
hypertension arising in
liver disease and portal
hypertension
• Excessive pulmonary
Vasoconstriction and
vascular remodeling
• Dyspnea, clubbing of the
Liver Failure
Gambaran Klinis
Hipertensi Portal
 Liver Failure
3. Acute on Chronic Liver Disease
Some individuals with stable but well-compensated,
advanced chronic liver disease, suddenly develop signs of
acute liver failure
• Chronic hepatitis B, superinfected with hepatitis D
• Medically suppressed hepatitis B infection - viral
mutants - resistant to therapy
• Sistemic event : sepsis, AHF, drug/toxic innjury, etc
 Liver Failure
Klasifikasi Sirosis berdasarkan morfologi :
1. Sirosis mikronoduler
Nodulus dg besar yang hampir seragam ± 3 mm
2. Sirosis makronoduler
Nodulus dg besar yang berbeda2 ± 1 cm
3. Sirosis bentuk campuran
 Liver Failure
Klasifikasi Sirosis Hepatis berdasarkan etiologi:
1. Akuisita
a. Sirosis alkoholik
b. Sirosis post hepatitis
c. Sirosis biliaris
d. Sirosis kardiak
2. Sirosis kongenital
a. Hemokromatosis
b. Wilson disease
c. Defisiensi α-1 antitripsin
 Liver Failure
Sirosis Biliaris
▪ Akibat kolestasis lama dan menetap.
▪ 2 bentuk :
▪ Sirosis biliaris primer
(kerusakan saluran empedu intrahepatal dg etiologi
autoimun)
▪ Sirosis biliaris sekunder
Akibat lanjut obstruksi aliran empedu
(cont : Kolelitiasis, Ca caput pankreas)
 Liver Failure
Sirosis Biliaris
Kolestasis –
jaringan ikat
proliferasi –
saluran empedu
dapat pecah –
kebocoran
empedu
 Liver Failure
Sirosis Kardiak
▪ Akibat kongesti vena pasif kronik (Cont : dekompensasio
kordis dekstra) – Nutmeg Liver – Sirosis Kardia
▪ Nekrosis sentrolobuler – fibrosis sentral
 Liver Failure
a. Hemokromatosis
▪ Kelainan metabolisme Fe pada bayi – peningkatan abnormal
absorbsi Fe dari usus - penimbunan Fe pada jaringan
b. Wilson DIsease
▪ Defisiensi protein plasma pengikat Cu, peningkatan abnormal
absorbsi Cu di usus – penimbunan CU dalam jaringan hepar, otak,
ginjal
c. Defisiensi α-1 antitripsin
▪ Gangguan hepatosit dalam mensintesis glikoprotein α-1 antitripsin
– defisiensi – protease terus bekerja merusak jaringan
Liver Failure
 A 53-year-old man comes to the emergency department
because of marked hematemesis that has continued for the
past 3 hours. On physical examination, he has a temperature
of 35.9°C, pulse of 112/min, respirations of 26/min, and blood
pressure of 90/45 mm Hg. He has a distended abdomen with
a fluid wave, and the spleen tip is palpable. What liver disease
is most likely to be present in this patient?
(A) Cirrhosis
(B) Cholangiocarcinoma
(C) Massive hepatic necrosis
(D) Fatty change
(E) HAV infection
 A 53-year-old man comes to the emergency department
because of marked hematemesis that has continued for the
past 3 hours. On physical examination, he has a temperature
of 35.9°C, pulse of 112/min, respirations of 26/min, and blood
pressure of 90/45 mm Hg. He has a distended abdomen with
a fluid wave, and the spleen tip is palpable. What can cause
hematemesis in this patient?
(A) Hemorrhoids
(B) Ruptured esophagela varices
(C) Fatty change
(D) Chronic Gastritis with erosion
(E) Hepotopulmonary syndrome
Hb RBC normal (85%)
Hb RBC muda Ren

Mioglobin
Enzim2
20%
Bilirubin I / Unconjugated

Bilirubin II / Conjugated
Bilirubin Metabolism - Enterohepatic Circulation Sterkobilinogen
 Patologi Ikterus
Perbedaan Bilirubin I dan II
Bilirubin I / Indirek Bilirubin II / Direk
(Unconjugated Bilirubin) (Conjugated Bilirubin)

Ikterus : Gejala Kuning pada plasma,

kulit, mukosa akibat pigmen empedu,
Bilirubin memiliki afinitas tinggi
terhadap serabut elastin
 Patologi Ikterus
Klasifikasi Ikterus (Berdasar Lokasi Kelainan) :
1. Akibat Kenaikan produksi bilirubin
2. Akibat gangguan uptake bilirubin oleh hepar
3. Akibat gangguan konjugasi bilirubin
4. Akibat gangguan ekskresi bilirubin
5. Akibat campuran oleh karena penurunan fungsi hepar

Klasifikasi Ikterus Berdasar Hubungannya dg Hepar :

Prehepatik, Parenkimatosa, Obstruktif
 Patologi Ikterus
1. Akibat Kenaikan produksi bilirubin
a. Ikterus hemolitik
Peningkatan kerusakan eritrosit – Unconjugated bilirubin
↑↑
b. Diseritropoeitik (Shunt) Bilirubin
Destruksi prematur eritrosit di sumsung tulang -
Unconjugated bilirubin ↑ ↑

Unconjugated bilirubin terikat albumin (90%) –

Tidak larut air - tidak diekskresi di urin (acholuric jaundice)
– difusi ke jaringan – toxic injury – Otak : Kernikterus
 Patologi Ikterus
2. Gangguan uptake bilirubin oleh hepar
Gilbert disease : familial non hemolitik acholuric
(autosomal dominan)

3. Gangguan Konjugasi bilirubin

a. Ikterus neonatorum (defisiensi Glucuronyl transferase
pada prematuritas)
b. Crigler Najjar Syndrome (defisiensi Glucuronyl
transferase herediter)
 Patologi Ikterus
4. Gangguan Ekskresi bilirubin (Serum AF ↑)
a. Intrahepatik herediter
Sindroma dubin johnson, Sindroma rotor
b. Intrahepatik akuisita
Sirosis hepatis, Hepatotoxic drug - kolestasis
c. Ekstrahepatik
• Batu empedu
• Ca caput pankreas
• Ca duktus koledokus
• Kelainan saluran empedu
 Patologi Ikterus
5. Campuran akibat penurunan fungsi hati
a. Infeksi Virus
b. Toksin
c. Bahan kimia
Trauma pada heptosit – kerusakan hepatosit –
mengganggu aliran empedu dalam kanalikuli - kolestasis
Klasifikasi Berdasar
Jenis
Hiperbilirubinemia
HEPATITIS
 PATOLOGI RADANG HATI
1. Radang Hati tidak khas
a. Lewat aliran darah
(Cont : Endokraditis, septikemia)
b. Lewat saluran empedu
(Cont : Cholangtis - retrograd)
c. Penyebaran organ sekitar
(Contoh : Abses subphrenic, Abses retroperitoneal,
Cholecystitis)
 PATOLOGI RADANG HATI
2. Radang Hati khas
a. Hepatitis Virus Akut
– Dapat ditularkan lewat fecal-oral (Hepatitis virus A,
E) atau parenteral (Hepatitis virus B, C, D)
– Gambaran patologi :
lymphoplasmacytic (mononuclear) infiltrate, minimal
portal inflammation, lobular hepatitis
 PATOLOGI RADANG HATI
2. Radang Hati khas
b. Hepatitis Virus Akut dengan nekrosis masif
– Penyebab : Komplikasi Hepatitis virus akut (Hep.A,
B), bahan kimia
– Gambaran patologi :
Nekrosis hepatosit luas, infiltrasi sel radang
c. Hepatitis Virus Jenis Lain
– Infeksi mononukleosis (EBV),
– Yellow fever (arbovirus grup B)
 PATOLOGI RADANG HATI
2. Radang Hati khas
d. Hepatitis Virus Kronik
– Radang hati menetap 6 bulan tanpa perbaikan,
etiologi : Virus, obat, unknown
– Gambaran patologi :
mononuclear portal infiltration.
Hepatitis kronik persisten (terbatas pada daerah
periportal), Hepatitis kronik aktif (Lebih luas – fibrosis
- sirosis) – piecemeal necrosis, dimulai daerah
periportal kemudian meluas
PATOLOGI RADANG HATI
PATOLOGI RADANG HATI
PATOLOGI RADANG HATI
PATOLOGI RADANG HATI
 PATOLOGI RADANG HATI
2. Radang Hati khas
e. Hepatitis Non Virus
Leptospirosis, Sifilis, TBC, Aktinomikosis, Amoebiasis,
Malaria, Kalaazar, Clonorchiasis dan Fasciolasis
PATOLOGI RADANG HATI
PATOLOGI RADANG HATI
HEPATITIS VIRUS
B
PATOLOGI RADANG HATI
PATOLOGI RADANG HATI
PATOLOGI RADANG HATI
 PATOLOGI RADANG HATI

Direct cell toxicity :

• Hepatic conversion of xenobiotic to active toxin / immune
mechanisms
 Alcoholic Liver Disease
• Alcohol accounts for 3.8% of deaths globally - 8th highest risk factor
for death
• Alcoholic liver injury :
1. Hepatocellular steatosis or fatty change
2. Alcoholic (or steato-) hepatitis
3. Steatofibrosis
• 80 mg/day alcohol : threshold for development of alcoholic liver
disease
• Multiple pathologic effects:
Changes in lipid metabolism, decreased export of
lipoproteins, and cell injury caused by reactive oxygen
species and cytokines
Alcoholic Liver Disease
Alcoholic Liver Disease

Alcoholic (Steato-) Hepatitis

 Alcoholic Liver Disease

Alcoholic steatosis and steatofibrosis

Lipid droplets accumulate in hepatocytes, Some fibrosis is present
Alcoholic Liver Disease

Alcoholic Cirrhosis
 Metabolic Liver Disease
Nonalcoholic Fatty Liver Disease (NAFLD)
• Spectrum of disorders that have in common the presence
of hepatic steatosis (fatty liver) in individuals who do not
consume alcohol
• Pathogenesis :
1. Insulin resistance (metabolic syndrome)- Eat more fast
food, less exercise - hepatic steatosis
2. Hepatocellular oxidative injury
Necrosis and the inflammatory reactions
 Metabolic Liver Disease
Nonalcoholic Fatty Liver Disease (NAFLD)
• Show all the changes associated with alcoholic liver
disease
 Metabolic Liver Disease
Nonalcoholic Fatty Liver Disease (NAFLD)
Three weeks after a meal at the Trucker's Cafe, a 28-year-old man
develops malaise, fatigue, and loss of appetite. He notes passing dark
urine. On physical examination, he has mild scleral icterus and right
upper quadrant tenderness. Laboratory studies show serum AST of 62
U/L and ALT of 58 U/L. The total bilirubin concentration is 3.9 mg/dL,
and the direct bilirubin concentration is 2.8 mg/dL. His symptoms abate
over the next 3 weeks. On returning to the cafe, he finds that it has
been closed by the city's health department. Which of the following
serologic test results is most likely to be positive in this patient?
 (A) Anti-HBs
 (B) IgM anti-HDV
 (C) Anti-HCV
 (D) IgM anti-HAV
 (E) Anti-HBc
A 51-year-old man has had increasing malaise and swelling of the lower
legs for the past 4 months. On physical examination, he is afebrile and
normotensive. There is pitting edema to the knees. The abdomen is
slightly distended with a fluid wave, but there is no tenderness. The liver
span is increased. Laboratory studies show total serum protein of 5
g/dL, albumin of 2.2 g/dL, AST of 65 U/L, ALT of 65 U/L, alkaline
phosphatase of 93 U/L, and total bilirubin of 1.8 mg/dL. A liver biopsy is
done; the figure shows the microscopic appearance of a
trichrome-stained specimen. Ingestion of which of the following is most
likely to have caused this illness?
(A) Acetaminophen
(B) Allopurinol
(C) Aspirin
(D) Ethanol
(E) Ferrous sulfate
 KOLESTASIS
• Accumulation of bile pigment in hepatic parenchyma
• Caused by extrahepatic / intrahepatic obstruction of bile
channels / defects in hepatocyte bile secretion
• Clinical features : jaundice, pruritus, skin xanthomas,
nutritional deficiencies of the fat-soluble vitamins
• Including : Large bile duct obstruction, Primary
hepatolithiasis, Neonatal cholestasis (ex: Atresia Biliaris),
Primary biliary cholangitis, Primary sclerosing cholangitis
KOLESTASIS
 KOLESTASIS

Bile plug
ductules

Ductular
proliferation Portal
expanded

Portal mixed
inflammation
 Primary Biliary Cholangitis (PBC)
• Autoimmune disease characterized by nonsuppurative,
inflammatory destruction of small and medium- sized
intrahepatic bile ducts
• 90% female, >50 y.o
• 95% AMA-positive, 50% ANA-positive, 40% ANCA-positive
 Primary Biliary Cholangitis (PBC)

Liver enlargement, nodularity Infiltrate of lymphocytes

cirrhosis, green discoloration - and plasma cells 
cholestasis
Hepatic Circulatory Disorders
 Hepatic Circulatory Disorders
Passive Congestion and Centrilobular Necrosis
 Hepatic Disease Associated with Pregnancy
• Hepatic diseases may occur in women with chronic liver
disease who become pregnant / develop during pregnancy
in women who were not affected by liver disease.
• Abnormal liver tests occur in 3% to 5% of pregnancies.
• Viral hepatitis (HAV, HBV, HCV, or HBV + HDV) is the most
common cause of jaundice in pregnancy.
• HEV Infection : more severe course in pregnant patients –
20% mortality
• 0,1% pregnant women : hepatic complications develop :
preeclampsia and eclampsia; acute fatty liver of
pregnancy, and intrahepatic cholestasis of pregnancy
Hepatic Disease Associated with Pregnancy
• 3% to 5% of pregnancies
• widespread maternal
Preeclampsia & endothelial dysfunction &
Eclampsia increased vascular
permeability
• Preeclampsia :
Hypertension, proteinuria,
Eclampisa : hyperreflexia
and convulsions
• HELLP syndrome :
Hemolysis, Elevated Liver
enzymes, and Low Platelets
• Intraparenchymal &
Subcapsular hematoma
dissecting under Glisson
capsule
 Hepatic Disease Associated with Pregnancy
Acute Fatty Liver of Pregnancy
• Spectrum of disorders ranging from subclinical or modest
hepatic dysfunction (elevated serum ALT, AST) to hepatic
failure, coma, and death
• 1 in 13,000 deliveries
• Pathogenesis : unknown - mitochondrial dysfunction
• Diffuse microvesicular steatosis, portal tract inflammation
 Hepatic Disease Associated with Pregnancy
Intrahepatic Cholestasis of Pregnancy
• Pruritus in the third trimester, darkening of urine, light
stools, jaundice, Serum bilirubin (mostly conjugated)
increased, alkaline phosphatase increased
• The altered hormonal state of pregnancy seems to combine
with biliary defects in the secretion of bile salts or sulfated
progesterone metabolites - cholestasis
 PATOLOGI SALURAN EMPEDU - Radang
• Kolangitis : radang pada saluran empedu
• Kolesistitis : radang pada kandung empedu (akut / kronik)

Penyebab :
▪ Kerusakan akibat rangsangan kimiawi cairan empedu yang
pekat, disertai obstruksi (Batu)
▪ Infeksi bakteri (Streptococus, bacillus, staphylococcus)
▪ Refluks enzym pakreas ke saluran empedu
 PATOLOGI SALURAN EMPEDU - Radang
Kolesistitis Akut
• Kandung empedu bengkak, empyema
• 80% dijumpai batu didalamnya
• Dinding kandung empedu menebal 10X lipat
• Infiltrasi sel radang, dapat menjadi kronik
 PATOLOGI SALURAN EMPEDU - Radang
Kolesistitis Kronik
• Kandung empedu menjadi lebih kecil / normal
• 80% dijumpai batu didalamnya
• Dinding kandung empedu menebal <5X lipat
• Infiltrasi sel radang kronik, fibrosis, Rokitansky-Aschoff
sinus (contains bile)
 PATOLOGI SALURAN EMPEDU - Radang

Infiltrated by inflammatory cells, Outpouching of the mucosa

through the muscularis wall forms Rokitansky-Aschoff sinus
 PATOLOGI SALURAN EMPEDU - Radang
Kolesterolosis
• Nama lain : “strowberrygall baldder”
• Penimbunan fokal kolesterol di epitel kandung empedu
• Gangguan metabolisme lokal, tanpa hiperkolesterolemia
• Biasanya tanpa gejala
 PATOLOGI SALURAN EMPEDU - Radang
Hidrops kandung empedu
• Terdapat sekresi lendir cair jernih dalam kandung empedu
• Penyebab : kolesistitis yang disertai obstruksi duktus
sistikus
• Empedu di dalam kantung diserap, kemudian diganti lendir
yang disekresikan dinding kandung empedu
• Gejala tidak seberat kolesistitis akut
 PATOLOGI SALURAN EMPEDU - Radang
kolelitiasis
• Pembentukan batu di kandung empedu / saluran
empedu
• Biasanya dijumpai pada koleistitis kronis / dapat
terjadi tanpa radang sebelumnya
• Jenis batu empedu :
a. Batu kolesterol (Bilirubin & kolesterol)
b. Batu Pigmen (Kalisium bilirubinat)
c. Batu kalsium karbonat (jarang)
 PATOLOGI SALURAN EMPEDU - Radang
kolelitiasis
• Faktor resiko – 4F :
a. Female : wanita banding pria = 4 : 1
b. Fat : pada wanita gemuk
c. Forty : Berusia 40 tahun atau lebih
d. Fertile : biasanya pada multipara
• Faktor predisposisi : anemia dan DM
PATOLOGI SALURAN EMPEDU - Radang
 PATOLOGI SALURAN EMPEDU - Radang
kolelitiasis
• Patogenesis :
a. Abnormalitas komposisi cairan empedu
Kenaikan kadar beberapa komponen dalam empedu (Cont :
anemia hemolitik – batu pigmen; Batu kolesterol – mengikat
kolesterol lebih banyak dg adanya garam empedu dan lesitin)
b. Radang
Pembentukan batu dapat terjadi setelah adanya peradangan
c. Stasis
Stasis – predisposisi infeksi bakteri – absorpsi air ↑ -
empedu lebih pekat – ketidakseimbangan komposisi
cairan empedu
 PATOLOGI SALURAN EMPEDU - Radang
kolelitiasis
Sifat batu :
1. Batu kolesterol
– 10 % dari semua batu = batu murni, Pasien tidak selalu
hiperkolesterolemia
– Terjadi akibat gangguan metabolisme kolesterol
– Besar, abu-kekuningan, biasanya tunggal, ringan
2. Batu Pigmen
– Jarang. Biasanya pada penyakit dg kadar bilirubin >>
– Umumnya ganda, ukuran sama, kecil hitam, rapuh
 PATOLOGI SALURAN EMPEDU - Radang
kolelitiasis
Sifat batu :
3. Batu Kalsium Karbonat
– Paling jarang
– Putih keabuan, halus seperti beras
4. Batu campuran
– Paling sering (90%), terdiri dari ketiga bentuk batu
diatas, umumnya inti batu murni, lapisannya campuran
– Warna, tergantung dominan. Hitam (bilirubin), Kuning
(kolesterol), Putih (karbonat)
 PATOLOGI SALURAN EMPEDU - Radang
kolelitiasis
 PATOLOGI SALURAN EMPEDU - Radang
Kolelitiasis
Komplikasi :
- Kolesistitis akut / kronik
- Obstruksi total
- Jika pada duktus sistikus : hidrops
- Jika pada duktus koledokus : kolangitis ascenden,
ikterus, sirosis bilier
- Jika dalam kandung empedu : kandung empedu
mengecil krn fibrosis pada kolesistitis kronik
- Perforasi kandung empedu
A 47-year-old man has experienced intermittent upper abdominal pain
for several weeks. Physical examination yields no remarkable findings.
Laboratory findings show total serum protein of 7.3 g/dL, albumin of 5.2
g/dL, total bilirubin of 7.5 mg/dL, direct bilirubin of 6.8 mg/dL, AST of 35
U/L, ALT of 40 U/L, and alkaline phosphatase of 207 U/L. A liver biopsy is
done, and microscopic examination of the specimen shows
intracanalicular cholestasis in the centrilobular regions, swollen liver
cells, and portal tract edema. There is no necrosis and no fibrosis. There
is no increase in stainable iron.
What is the most likely diagnosis?
(A) Chronic passive congestion
(B) HBV infection
(C) Choledocholithiasis
(D) Extrahepatic biliary atresia
(E) Veno-occlusive disease
SELAMAT BELAJAR